Fasciolosis

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Fasciolosis
ICD-10 B66.3
ICD-9 121.3
DiseasesDB 4757
eMedicine ped/760 
MeSH D005211

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Fasciolosis is an important helminth disease caused by two trematodes Fasciola hepatica (the common liver fluke) and Fasciola gigantica. This disease belongs to the plant-borne trematode zoonoses. In Europe, the Americas and Oceania only F. hepatica is a concern, but the distributions of both species overlap in many areas of Africa and Asia.[1]

The definitive host range is very broad and includes many herbivorous mammals, including humans. The life cycle includes freshwater snails as an intermediate host of the parasite.[2] Recently, worldwide losses in animal productivity due to fasciolosis were conservatively estimated at over US$3.2 billion per annum.[3] In addition, fasciolosis is now recognized as an emerging human disease: the World Health Organization (WHO) has estimated that 2.4 million people are infected with Fasciola, and a further 180 million are at risk of infection.[4]

File:Fasciola hepatica.JPG
Fasciola hepatica

Source of infection for humans and transmission

Human F. hepatica infection is determined by the presence of the intermediate snail hosts, domestic herbivorous animals, climatic conditions and the dietary habits of man.[5] Sheep, goats and cattle are considered the predominant animal reservoirs. While other animals can be infected, they are usually not very important for human disease transmission. On the other hand, some authors have observed that donkeys and pigs contribute to disease transmission in Bolivia.[6] Among wild animals, it has been demonstrated that the peridomestic rat (Rattus rattus) may play an important role in the spread as well as in the transmission of the parasite in Corsica.[7] In France, nutria (Myocastor coypus) was confirmed as a wild reservoir host of F. hepatica.[8] Humans are infected by ingestion of aquatic plants that contain the infected metacercariae.[9] Several species of aquatic vegetables are known as a vehicle of human infection. In Europe, Nasturtium officinale (common watercress), N. silvestris, Rorippa amphibia (wild watercress), Taraxacum dens leonis (dandelion leaves), Valerianella olitora (lamb’s lettuce), and Mentha viridis (spearmint) were reported as a source of human infections.[10] In the Northern Bolivian Altiplano, some authors suggested that several aquatic plants such as bero-bero (watercress), algas (algae), kjosco and tortora could act as a source of infection for humans.[11] Because F. hepatica cercariae also encyst on water surface, humans can be infected by drinking of fresh untreated water containing metacercariae.[5] In addition, an experimental study suggested that humans consuming raw liver dishes from fresh livers infected with juvenile flukes could become infected.[12]

Intermediate hosts

File:Galba truncatula.jpg
Galba truncatula - the most common intermediate host of F. hepatica in Europe and South America

Intermediate hosts of F. hepatica are freshwater snails from family Lymnaeidae.[2][13] Snails from family Planorbidae act as an intermediate host of F. hepatica very occasionally.[1]

More reading in Fasciola hepatica

Pathogenesis

Clinical Signs

In humans

File:F. hepatica hypertrophia of bile duct.jpg
Hypertrophia of bile ducts in liver caused by F. hepatica (liver section; goat)
File:F. hepatica adults in bile duct.jpg
Adult flukes Fasciola hepatica in bile ducts (liver of goat)

The course of fasciolosis in humans has 4 main phases:[10]

  • Incubation phase: from the ingestion of metacercariae to the appearance of the first symptoms; time period: few days to 3 months; depends on number of ingested metacercariae and immune status of host
  • Invasive or acute phase: fluke migration up to the bile ducts. This phase is a result of mechanical destruction of the hepatic tissue and the peritoneum by migrating juvenile flukes causing localized and or generalized toxic and allergic reactions.[14] The major symptoms of this phase are:
  • Latent phase: This phase can last for months or years. The proportion of asymptomatic subjects in this phase is unknown. They are often discovered during family screening after a patient is diagnosed.[10]
  • Chronic or obstructive phase:

This phase may develop months or years after initial infection. Adult flukes in the bile ducts cause inflammation and hyperplasia of the epithelium. The resulting cholangitis and cholecystitis, combined with the large body of the flukes, are sufficient to cause mechanical obstruction of the biliary duct. In this phase, biliary colic, epigastric pain, fatty food intolerance, nausea, jaundice, pruritus, right upper-quadrant abdominal tenderness, etc., are clinical manifestations indistinguishable from cholangitis, cholecystitis and cholelithiasis of other origins. Hepatic enlargement may be associated with an enlarged spleen or ascites. In case of obstruction, the gall bladder is usually enlarged and edematous with thickening of the wall. Fibrous adhesions of the gall bladder to adjacent organs are common. Lithiasis of the bile duct or gall bladder is frequent and the stones are usually small and multiple.[10]

In animals

Clinical signs of fasciolosis are always closely associated with infectious dose (amount of ingested metacercariae). In sheep, as the most common definitive host, clinical presentation is divided into 4 types:[15][16]

  • Acute Type I Fasciolosis: infectious dose is more than 5000 ingested metacercariae. Sheep suddenly die without any previous clinical signs. Ascites, abdominal haemorrhage, icterus, pallor of membranes, weakness may be observed in sheep.
  • Acute Type II Fasciolosis: infectious dose is 1000-5000 ingested metacercariae. As above, sheep die but briefly show pallor, loss of condition and ascites.
  • Subacute Fasciolosis: infectious dose is 800-1000 ingested metacercariae. Sheep are lethargic, anemic and may die. Weight loss is dominant feature.
  • Chronic Fasciolosis: infectious dose is 200-800 ingested metacercariae. Asymptomatic or gradual development of bottle jaw and ascites (ventral edema), emaciation, weight loss.

In blood, anemia, hypoalbuminemia, and eosinophilia may be observed in all types of fasciolosis.[16] Elevation of liver enzyme activities, such a glutamate dehydrogenase (GLDH), gamma-glutamyl transferase (GGT), and lactate dehydrogenase (LDH), is detected in subacute or chronic fasciolosis from 12-15 week after ingestion of metacercariae.[17][18] Economical effect of fasciolosis in sheep consists in sudden deaths of animals as well as in reduction of weight gain and wool production.[19][20] In goats and cattle, the clinical manifestation is similar to sheep. However, acquired resistance to F. hepatica infection is well-known in adult cattle.[21][22] Calves are susceptible to disease but in excess of 1000 metacercariae are usually required to cause clinical fasciolosis. In this case the disease is similar to sheep and is characterized by weight loss, anemia, hypoalbuminemia and (after infection with 10,000 metacercariae) death.[23] Importance of cattle fasciolosis consist in economic losses caused by condemnation of livers at slaughter and production losses especially due to reduced weight gain.[24]

Resistance to infection

Mechanisms of resistance have been studied by several authors in different animal species. These studies may help to better understand the immune response to F. hepatica in host and are necessary in development of vaccine against the parasite. It has been established that cattle acquire resistance to challenge infection with F. hepatica and F. gigantica when they have been sensitized with primary patent or drug-abbreviated infection.[21] Resistance to fasciolosis was also documented in rats.[25] On the other hand, sheep and goats are not resistant to re-infection with F. hepatica.[26][27] However, there is evidence that two sheep breeds, in particular Indonesian thin tail sheep and Red maasai sheep, are resistant to F. gigantica.[28][29] No reports concerning the resistance in humans are available.

Diagnosis

In humans, diagnosis of fasciolosis is usually achieved by parasitologically by findings the fluke eggs in stool, and immunologically by ELISA and Western blot. Coprological examinations of stool alone are generally not adequate because infected humans have important clinical presentations long before eggs are found in the stools. Moreover, in many human infections, the fluke eggs are often not found in the faeces, even after multiple faecal examinations.[30][5] Furthermore, eggs of F. hepatica, F. gigantica and Fasciolopsis buski are morphologically indistinguishable.[30] Therefore, immunonological methods such ELISA and enzyme-linked immunoelectrotransfer blot, also called Western blot, are the most important methods in diagnosis of F. hepatica infection. These immunological tests are based on detection of species-specific antibodies from sera. The antigenic preparations used have been primarily derived from extracts of excretory/secretory products from adult worms, or with partially purified fractions.[31] Recently, purified native and recombinant antigens have been used, e.g. recombinant F. hepatica cathepsin L-like protease.[32] Methods based on antigen detection (circulating in serum or in faeces) are less frequent. In addition, biochemical and haematological examinations of human sera support the exact diagnosis (eosinophilia, elevation of liver enzymes). Ultrasonography and RTG of the abdominal cavity, biopsy of liver, and gallbladder punctuate can also be used. False fasciolosis (pseudofasciolosis) refers to the presence of eggs in the stool resulting not from an actual infection but from recent ingestion of infected livers containing eggs. This situation (with its potential for misdiagnosis) can be avoided by having the patient follow a liver-free diet several days before a repeat stool examination.[31] In animals, intravital diagnosis is based predominantly on faeces examinations and immunological methods. However, clinical signs, biochemical and haematological profile, season, climate conditions, epidemiology situation, and examinations of snails must be considered.[2][15] Similarly to humans, faeces examinations are not reliable. Moreover, the fluke eggs are detectable in faeces 8-12 weeks post-infection. In spite of that fact, faecal examination is still the only used diagnostic tool in some countries. While coprological diagnosis of fasciolosis is possible from 8-12 week post-infection (WPI) F. hepatica specific-antibodies are recognized using ELISA or Western blot since 2-4 week post-infection.[33][34] Therefore, these methods provide early detection of the infection.

Treatment and prevention

Anthelmintics

In humans

For high efficacy and safety, triclabendazole (Egaten®) in dose 10-12 mg/kg is drug of choice in human fasciolosis.[35] No drug alternatives are available for humans. On the other hand, nitazoxanide were successfully used in human fasciolosis treatment in Mexico.[36] Bithionol is another drug of choice used for treatment of fasciola hepatica.[37]

In animals

Formula of triclabendazole

A number of drugs have been used in control fasciolosis in animals. Drugs differ in their efficacy, mode of action, price, and viability. Fasciolicides (drugs against Fasciola spp.) fall into five main chemical groups:[38]

Triclabendazole (Fasinex) is considered as the most common drug due to its high efficacy against adult as well as juvenile flukes. Triclabendazole is used in control of fasciolosis of livestock in many countries. Nevertheless, long-term veterinary use of triclabendazole has caused appearance of resistance to F. hepatica. In animals, triclabendazole resistance was first described in Australia,[39] later in Ireland[40] and Scotland[41] and more recently in the Netherlands.[42] Considering this fact, scientists have started to work on the development of new drug. Recently, a new fasciolicide was successfully tested in naturally and experimentally infected cattle in Mexico. This new drug is called compound Alpha and is chemically very much closed to triclabendazole.[43]

References

  1. ↑ 1.0 1.1 Mas-Coma, S., Bargues, M.D., Valero, M.A., 2005. Fascioliasis and other plant-borne trematode zoonose. Int. J. Parasitol. 35, 1255–1278.
  2. ↑ 2.0 2.1 2.2 Torgerson, P., Claxton, J., 1999. Epidemiology and control. In: Dalton, J.P. (Ed.), Fasciolosis. CAB International Publishing, Wallingford, pp. 113–149.
  3. ↑ Spithill, T.W., Smooker, P.M., Copeman, D.B. 1999. Fasciola gigantica: epidemiology, control, immunology and molecular biology. In: Dalton, J.P. (Ed.), Fasciolosis. CAB International Publishing, Wallingford, pp. 465–525.
  4. ↑ Anonymus 1995. Control of Foodborne Trematode Infections. WHO Technical Series No. 849. WHO, Geneva, 157 pp.
  5. ↑ 5.0 5.1 5.2
  6. ↑ Mas-Coma, S., Rodriguez, A., Bargues, M.D., Valero, M.A., Coello, J., Angles, R., 1998. Secondary reservoir role of domestic animals other than sheep and cattle in fascioliasis transmission on the northern Bolivian Altiplano. Res. Rev. Parasitol. 57, 39–46.
  7. ↑ Mas-Coma, S., Fons, R., Feliu, C., Bargues, M.D., Valero, M.A., Galán-Puchades, M.T., 1988. Small mammals as natural definitive hosts of the liver fluke, Fasciola hepatica Linnaeus, 1758 (Trematoda: Fasciolidae): a review and two new records of epidemiologic interest on the island of Corsica. Rivista di Parassitologia 5, 73–78.
  8. ↑ Menard, A., Agoulon, A., L’Hostis, M., Rondelaud, D., Collard, S., Chauvin, A., 2001. Myocastor coypus as a reservoir host of Fasciola hepatica in France. Vet. Res. 32, 499–508.
  9. ↑ Markell, E.K., Voge, M., 1999. Medical Parasitology, eighth ed.. Saunders Company Publication, pp. 185–188.
  10. ↑ 10.0 10.1 10.2 10.3
  11. ↑ Bjorland, J., Bryan, R.T., Strauss, W., Hillyer, G.V., McAuley, J.B., 1995. An outbreak of acute fascioliasis among Aymara Indians in the Bolivian Altiplano. Clin. Infect. Dis. 21, 1228–1233.
  12. ↑ Taira, N., Yoshifuji, H., Boray, J.C., 1997. Zoonotic potential of infection with Fasciola spp. by consumption of freshly prepared raw liver containing immature flukes. Int. J. Parasitol. 27, 775–779.
  13. ↑ Graczyk, T.K., Fried, B., 1999. Development of Fasciola hepatica in the intermediate host. In: Dalton, J.P. (Ed.), Fasciolosis. CAB International Publishing, Wallingford, pp. 31–46.
  14. ↑ Facey, R.V., Marsden, P.D., 1960. Fascioliasis in man: an outbreak in Hampshire. Brit. Med. J. ii, 619–625.
  15. ↑ 15.0 15.1
  16. ↑ 16.0 16.1
  17. ↑ Anderson, P.H., Matthews, J.G., Berrett, S., Brush, P.J., Patterson, D.S., 1981. Changes in plasma enzyme activities and other blood components in response to acute and chronic liver damage in cattle. Res Vet Sci. 31, 1-4.
  18. ↑ Sykes, A.R., Coop, A.R., Robinson, M.G., 1980. Chronic subclinical ovine fascioliasis: plasma glutamate dehydrogenase, gamma glutamyl transpeptidase and aspartate aminotransferase activities and their significance as diagnostic aids. Res. Vet. Sci. 28, 71–78.
  19. ↑ Sinclair, K.B., 1962. Observations on the clinical pathology of ovine fascioliasis. Brit. Vet. J. 118, 37–53.
  20. ↑ Roseby, F.B. 1970. The effect of fasciolosis on the wool production of merino sheep. Aust. Vet. J. 46, 361–365.
  21. ↑ 21.0 21.1 Haroun, E.M., Hillyer, G.V., 1986. Resistance to fascioliasis – a review. Vet. Parasitol. 20, 63–93.
  22. ↑ Doyle, J.J., 1973. The relationship between the duration of a primary infection and the subsequent development of an acquired resistance to experimental infections with Fasciola hepatica in calves. Res. Vet. Sci., 14, 97-103.
  23. ↑
  24. ↑ Phiri, I.K., Phiri, A.M., Harrison, L.J.S., 2006. Serum antibody isotype responses of Fasciola-infected sheep and cattle to excretory and secretory products of Fasciola species. Vet. Parasitol. 141, 234–242.
  25. ↑ Van Milligen, F.J., Cornelissen, J.B.W.J., Bokhout, B.A., 1998. Location of induction and expression of protective immunity against Fasciola hepatica at the gut level: a study using an ex vivo infection model with ligated gut segments. J. Parasitol. 84, 771–777.
  26. ↑ Chauvin, A., Bouvet, G., Boulard, C., 1995. Humoral and cellular immune responses to Fasciola hepatica experimental primary and secondary infection in sheep. Int. J. Parasitol. 25, 1227-41.
  27. ↑ Martinez-Moreno, A., Martínez-Moreno, F.J., Acosta, I., Gutiérrez, P.N., Becerra, C., Hernández, S. 1997. Humoral and cellular immune responses to experimental Fasciola hepatica infections in goats. Parasitol. Res. 83, 680–686.
  28. ↑ Roberts, J.A., Estuningsih, E., Wiedosari, E., Spithill, T.W., 1997. Acquisition of resistance against Fasciola gigantica by Indonesian thin tail sheep. Vet. Parasitol. 73, 215–224.
  29. ↑ Wamae, L.W., 1996. Comparative pathogenesis and immunochemistry analysis of Fasciola gigantica infection in cattle and sheep. PhD Thesis. University of Edinburgh.
  30. ↑ 30.0 30.1 Hillyer, G.V., 1988. Fascioliasis and fasciolopsiasis. In: Balows, A., Hausler, W.J., Ohashi, M. and Turano, A. (eds) Laboratory Diagnosis of Infectious Diseases. Principles and Practice. I. Bacterial, Mycotic, and Parasitic Diseases, Vol. 90. Springer-Verlag, Berlin, pp. 856–862.
  31. ↑ 31.0 31.1 Hillyer, G.V., 1999. Immunodiagnosis of human and animal fasciolosis. In: Dalton, J.P. (Ed.), Fasciolosis. CAB International Publishing, Wallingford, pp. 435–447.
  32. ↑ O’Neill, S.M., Parkinson, M., Strauss, W., Angles, R., Dalton, J.P., 1998. Immunodiagnosis of Fasciola hepatica infection (fasciolosis) in a human population in the Bolivian Altiplano using purified cathepsin L cysteine proteinase. Am. J. Trop. Med. Hyg. 58, 417–423.
  33. ↑ Zimmerman, G.L., Jen, L.W., Cerro, J.E., Farnsworth, K.L., Wescott, R.B., 1982. Diagnosis of Fasciola hepatica infections in sheep by an enzyme-linked immunosorbent assay. Am. J. Vet. Res. 43, 2097–2100.
  34. ↑ Duménigo, B.E., Espino, A.M., Finlay, C.M., Mezo, M., 2000. Kinetics of antibody-based antigen detection in serum and faeces of sheep experimentally infected with Fasciola hepatica. Vet. Parasitol. 89, 153-161.
  35. ↑ Savioli, L., Chistulo, L., Montresor, A., 1999. New opportunities for the control of fascioliasis. Bull. WHO 77, 300.
  36. ↑ Rossignol, J.F., Abaza, H., Friedman, H., 1998. Successful treatment of human fascioliasis with nitazoxanide. Trans. Roy. Soc. Trop. Med. Hyg. 92, 103–104.
  37. ↑ Ramachandran, A., 2000. Pharmacology Recall.
  38. ↑ Fairweather, I., Boray, J.C., 1999. Fasciolicides: efficacy, action, resistance and its management. Vet. J. 158, 81–112
  39. ↑ Overend, D.J., Bowen, F.L., 1995. Resistance of Fasciola hepatica to triclabendazole. Aust. Vet. J. 72, 275–6.
  40. ↑ O’Brien, D.J., 1998. Fasciolosis: a threat to livestock. Irish Vet. J. 51, 539–541.
  41. ↑ Mitchell, G.B., Maris, L., Bonniwell, M.A., 1998. Triclabendazole-resistant liver fluke in Scottish sheep. Vet. Rec. 143, 399.
  42. ↑ Moll, L., Gaasenbeek, C.P.H., Vellema, P., Borgsteede, F.H.M., 2000. Resistance of Fasciola hepatica against triclabendazole in cattle and sheep in the Netherlands. Vet. Rec. 91, 153–158.
  43. ↑ Ibarra, F., Vera, Y., Quiroz, H., Canto, J., Castillo, R., Hernandez, A., Ochoa, P. 2004. Determination of the effective dose of an experimental fasciolicide in naturally and experimentally infected cattle. Vet. Parasitol. 120, 65–74.

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